Studying the analytical performance of various commercial methods (two different ELISAs and an immunoturbidimetric method) for the measurement of lipoprotein(a), we observed analytically and clinically important differences in their standardization. In addition, we found evidence for apolipoprotein(a) isoform-dependence in at least two of three methods, that further questions their clinical utility. In a collaborative study, we studied the possible effect of frequent blood donations on the development of atherosclerosis in healthy adult blood donors. Despite reductions in body iron stores by frequent blood donation, there was no evidence for a reduced risk of atherosclerosis as assessed by carotid artery intimal thickness and a variety of multiple laboratory markers of inflammation. In another collaborative clinical study, we observed that combination of an HMG-CoA reductase inhibitor drug ("statin") with estrogen attenuates the increase in C-reactive protein during estrogen replacement therapy in postmenopausal women. This is of importance because elevated C-reactive protein levels may have inflammatory and thrombotic consequences that compromise any benefit to cardiovascular risk reduction by estrogens. In a third collaborative clinical study, we assessed the effect of hormone replacement therapy on carotid artery compliance in healthy postmenopausal women. We found that a 3-month hormone replacement therapy significantly improved the carotid artery compliance, as determined by magnetic resonance imaging (MRI) and blood pressure measurements. This effect was independent of changes in serum levels of lipids and markers of inflammation, including C-reactive protein. In a fourth collaborative clinical study, we studied the role of angiotensin II type 1 (AT1) receptor in the regulation of cellular adhesion molecules in atherosclerosis. We found that AT1 receptor antagonism induced by the administration of losartan (an AT1 receptor antagonist) selectively modulated the expression of L-selectin on leukocytes, while did not affect other leukocyte and serum adhesion molecules and C-reactive protein. L-selectin is a leukocyte adhesion molecule that is rapidly shed after leukocyte activation so it is often decreased in coronary artery disease. In still another collaborative clinical study, we continued studying the relationship between antibodies to various heat-shock proteins and coronary artery disease. Results of this study are being evaluated.